Introduction

Classification

Taxonomy

• Order: Rickettsiales; Family: Rickettsiaceae; Tribe: Rickettsieae.
• One of at least 18 members of the Spotted Fever Group organisms within the genus Rickettsia.

Active Forms

Clinical Effects

Epidemiology

Habitat

• Even in endemic areas, only 1-3% of susceptible ticks are infected with R rickettsii.
• Infections often occur in limited geographic pockets within endemic areas.
• Vector for transmission in the Eastern and Central USA is Dermacentor variabilis (American dog tick).
• Vectors for transmission in the western USA include both D variabilis (American dog tick)  and D andersonii (American wood tick/Rocky Mountain wood tick) .

Lifecycle

• Ticks can become infected during nymphal and larval stages while feeding on small mammals.
• Venereal transmission between ticks can occur at time of mating.
• Infection of ticks with R rickettsii is transtadial as well as transovarial. Infected ticks may remain infected during every stage of life.
• Transovarial transmission from female tick to her offspring is very efficient.
• Small mammals and ticks themselves serve as reservoirs of infection.
• Dogs do not serve as reservoirs of infection because of short duration, low level rickettsemia in this species.

Transmission

• R rickettsii can not be transmitted directly between dogs.
• R rickettsii is transmitted to dogs via salivary secretions during feeding of infected ticks.
• From 5 to 20 hours of feeding is required for reactivation of the organism prior to transmission.

Pathological effects

• See serum protein electrophoresis Serum protein electrophoresis.
• Serum IgM response becomes detectable at approximately 9 days post infection, peaks by day 20 and remains detectable for 2 to 3 months.
• Serum IgG response becomes detectable at approximately 25 days post infection, peaks by day 42 and gradually declines over 6 to 9 months.
• Immunological response to R rickettsii can result in elimination of infection.
• Challenge inoculation following experimental exposure failed to induce disease even 3 years after disease recovery.

• R rickettsii is inoculated through salivary secretions of an infected tick during feeding.
• After attachment and entry into endothelial cells, organism proliferates within cell cytosol and nuclei.
• Infection is spread centripetally from cell to cell in microcirculation of skin and organs.
• Intracellular endothelial infection results in central feature of the disease Rocky Mountain Spotted Fever Rocky Mountain Spotted Fever (RMSF) ; lymphocytic vasculitis.
• Disease pathology and complications result from vasculitis of microcirculation in a variety of tissues and organs.

Other Host Effects

• Fever results from both endogenous (especially inflammatory cytokines) and exogenous (bacterial cell wall components) pyrogens.
• Vasculitis leads to clinical manifestations including petechial hemorrhage, central nervous system signs, respiratory and gastrointestinal signs, peripheral edema and dermal necrosis.
• Vasculitis leads to clinicopathologic manifestations including thrombocytopenia, hypoalbuminemia Hypoproteinemia , and hyponatremia.

Control

Control via animal

• Prevention of tick attachment prevents disease transmission.
• Antimicrobial therapy Therapeutics: antimicrobial drug effective when administered early in disease course.
• Dogs not a significant reservoir of infection for other animals.

Control via chemotherapies

• Doxycycline Doxycycline dose, 5 mg/kg PO q 12 hours, 7 to 10 days.
• Alternative tetracycline compounds: tetracycline Tetracycline , oxytetracycline Oxytetracycline , minocycline Minocycline.
• Chloramphenicol Chloramphenicol , 15 to 20 mg/kg PO, IV, or IM q 8 hours.
• Enrofloxacin Enrofloxacin , 3 to 5 mg/kg PO or IM q 12 hours.

Control via environment

• Control accomplished by preventing attachment and feeding of ticks.

Vaccination

• No commercial vaccine available.

Diagnosis

Further Reading

Publications

Refereed papers

• Recent references from PubMed and VetMedResource.
• Gasser A M, Birkenheuer A J & Breitschwerdt E B (2001) Canine Rocky Mountain Spotted fever: a retrospective study of 30 cases. J Am Anim Hosp Assoc 37 (1), 41-48 PubMed.
• Hackstadt T (1996) The biology of Rickettsiae. Infect Agents & Dis 5 (3), 127-143 PubMed.
• Sexton D J, Kanj S S, Wilson K et al (1994) The use of a polymerase chain reaction as a diagnostic test for Rocky Mountain spotted fever. Am J Trop Med & Hygiene 50 (1), 59-63 PubMed.
• Breitschwerdt E B, Levy M G, Davidson M G et al (1990) Kinetics of IgM and IgG responses to experimental and naturally acquired Rickettsia rickettsii infection in dogs. Am J Vet Res 51 (8), 1312-1316 PubMed.
• Keenan K P, Buhles W C Jr., Huxsoll D L et al (1977) Pathogenesis of infection with Rickettsia rickettsii in the dog: a disease model for Rocky Mountian spotted fever. J Infect Dis 135 (6), 911-917 PubMed.
• Keenan K P, Buhles W C Jr., Huxsoll D L et al (1977) Studies on the pathogenesis of Rickettsia rickettsii in the dog: clinical and clinicopathologic changes of experimental infection. Am J Vet Res 38 (6), 851-856 PubMed.

Other sources of information

• Centers for Disease Control, National Center for Infectious diseases, 1600 Clifton Road NE, MS G-13, Atlanta, Georgia 30333, USA. www.cdc.gov/ncidod/dvrd/rmsf